Fig. 19.17 ). This release of O2 from blood is facilitated by the shift in the oxyhemoglobin dissociation curve during exercise. During exercise, the high concentration of CO2 and the formation of lactic acid cause a reduction in tissue pH. This decrease in pH, in addition to the increase in temperature in the contracting muscle, shifts the oxyhemoglobin dissociation curve to the right (see ). Therefore, at any given PO2, less O2 is held by the hemoglobin in the red blood cells, and consequently more O2 is available for the tissues. Oxygen consumption may increase as much as 60-fold, with only a 15-fold increase in muscle blood flow. Muscle myoglobin may serve as a limited O2 store during exercise, and it can release the attached O2 at very low partial pressures. However, myoglobin can also facilitate O2 transport from capillaries to mitochondria by serving as an O2 carrier.
Because the enhanced sympathetic drive and the reduced parasympathetic inhibition of the sinoatrial node continue during exercise, tachycardia persists. If the workload is moderate and constant, the heart rate reaches a certain level and remains there throughout the period of exercise. However, if the workload increases, the heart rate increases concomitantly until a plateau of approximately 180 beats per minute is reached during strenuous exercise. In contrast to the large increase in heart rate, the increase in stroke volume is only approximately 10% to 35%, the larger values occurring in trained individuals (see
Fig. 19.17 ). In well-trained distance runners, whose cardiac output can reach six to seven times the resting level, stroke volume attains approximately twice the resting value.
Cardiacmusclesize(growth)isdirectlyrelatedtotheamountofworkthatisimposeduponit.Duringdevelopmentandinenduranceexercise,cardiacgrowthisachievedataconstantrelationbetweensystolicbloodpressureandtheratioofwallthicknesstoventricularchamberradius.Anechocardiographicmeasurementusedtodistinguishphysiologicalfrompathologicalhypertrophyisrelativewallthickness(ratioofleftventricularwallthicknesstochamberradius).Inphysiologicalhypertrophy,leftventricularmassandradiusincreaseproportionatelysothatrelativewallthicknessdoesnotchangesignificantly.Examplesofphysiologicalhypertrophyoccurinenduranceathletesandinpregnantwomen,inwhomleftventricularenlargementoccurswithvolumeoverloadatconstantrelativewallthickness.Physiologicalhypertrophyisassociatedwithanincreasedarteriolardiameterinexperimentalanimals.Also,capillarydensityincreasesinproportiontothedegreeofhypertrophy.Thisisincontrasttothesituationinpathologicalhypertrophy,inwhichareductionofcapillarydensity(rarefaction)canoccur.Neithermyocardialfibrosisnorderangementofmusclefiberorientationisdetectedinphysiologicalhypertrophy,incontrasttothefindingsinpathologicalhypertrophy.
Thus the increase in cardiac output observed during exercise is correlated principally with an increase in heart rate. If the baroreceptors are denervated, the cardiac output and heart rate responses to exercise are small in comparison with those in individuals with normally innervated baroreceptors. However, with total cardiac denervation, exercise still increases cardiac output as much as it does in normal individuals. This increase in cardiac output is achieved chiefly by means of an elevated stroke volume. However, if a β-adrenergic receptor antagonist is given to dogs with denervated hearts, exercise performance is impaired. The β-adrenergic receptor antagonist prevents the cardiac acceleration and enhanced contractility caused by increased amounts of circulating catecholamines. Therefore, the increase in cardiac output necessary for maximal exercise performance is limited.